Chemicals such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and naturally occurring toxins such as the tricothecene mycotoxin, T2 toxin, adversely affect immunologic function in offspring following treatment of pregnant mice over various periods of gestation. Studies are in progress to explore the relationship between developmental immunotoxicity and the induction of structural malformations. These studies are, in particular, addressing the following question: Do modulations in lymphocytic surface antigens, induced by prenatal chemical exposure, result in functional immunologic deficits later in life? TCDD or T2 toxin are administered to pregnant C57Bl/6 and B6C3F1 mice during gestation to establish the sensitive period for induction of immunologic deficits and to identify the initial lesion. Fetal T and B lymphocytes from the spleen and thymus, and subpopulations of these cells, are stained immunocytochemically to determine the morphological effects of TCDD and T2 toxin on lymphocytic surface antigens and their development. Fetal thymic organ culture is used to determine effects of exposure on subpopulations of immune cells. In addition, cell populations are evaluated by flow cytometry to determine quantitative changes. If changes in these surface markers persist beyond the age of 4 weeks in the prenatally exposed animal, functional tests, including mixed lymphocyte reaction, plaque assay, in vitro blastogenesis, cytotoxic T lymphocyte function, and colony forming unit assay, are conducted.